In Escherichia coli K-12, mutations at a single locus result in a loss of coordination of DNA synthesis and cell division, of regulation of capsular polysaccharide synthesis and polypeptide breakdown and a decrease in the ability to inherit extrachromosomal elements, whether plasmids or prophage. Genetic evidence has raised the possibility that more than one gene is involved. The proposed research objectives include construction of a fine-structure genetic map of the lon locus and determination of the complementation pattern between different lon mutations to determine whether the locus includes one or two (or more) genes. The isolation and characterization of Lon suppressor mutations can contribute towards an understanding of the targets of lon-gene(s) action. Finally, identification and cellular localization of the lon-locus product(s) will lead to a method to follow regulation of the lon-locus product(s). These studies will serve as a basis to formulate a molecular model of the coordination of DNA replication and cell division as well as regulation of capsular polysaccharide synthesis, polypeptide breakdown, and inheritance of extrachromosomal genetic determinants. Further, they can serve to guide research of other loci involved in multiple regulatory functions. Finally, because of the roles of capsular polysaccharide and plasmid-borne antibiotic resistance in infectious disease, this research has significance for public health.